No influence of presenilin 1 I143T and G384A mutations on endogenous tau phosphorylation in human and mouse neuroblastoma cells

Presenilin 1 (PSEN1) I143T and G384A mutations give rise to severe early-onset Alzheimer's disease in two extensively studied Belgian families. In the present study, we examined the effect of PSEN1 I143T and G384A mutations on tau phosphorylation in human SH-SY5Y and mouse Neuro-2a neuroblastom...

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Bibliographic Details
Published in:Neuroscience letters 1999-07, Vol.269 (2), p.83-86
Main Authors: JULLIAMS, A, VANDERHOEVEN, I, KUHN, S, VAN BROECKHOVEN, C, DE JONGHE, C
Format: Article
Language:English
Subjects:
Biological and medical sciences
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Medical sciences
Neurology
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Summary:Presenilin 1 (PSEN1) I143T and G384A mutations give rise to severe early-onset Alzheimer's disease in two extensively studied Belgian families. In the present study, we examined the effect of PSEN1 I143T and G384A mutations on tau phosphorylation in human SH-SY5Y and mouse Neuro-2a neuroblastoma cell lines that were transiently transfected with wild type (WT) or mutant PSEN1. With a phosphorylation independent antibody, no alteration in the electrophoretic mobility of tau was observed between wild type and mutant PSEN1 transfectants. Also, densitometric analysis of Tau1 immunoreactivity, characteristic of unphosphorylated tau, demonstrated no significant differences between WT and mutant PSEN1 transfectants. Our data suggest that in the cellular models we used, transient overexpression of I143T and G384A mutant PSEN1 does not lead to increased tau phosphorylation.
ISSN:0304-3940
1872-7972
DOI:10.1016/S0304-3940(99)00402-4